ReviewBrain pathology (Zurich, Switzerland)1998
p53 and brain tumors: from gene mutations to gene therapy.
Review in Brain pathology (Zurich, Switzerland), 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 82 citations in OpenAlex.
- Graphene quantum dot-integrated nanocomposites: a promising avenue for glioblastoma treatment.Medical oncology (Northwood, London, England) · 2025Review
- Distinct expression and function of breast cancer metastasis suppressor 1 in mutant P53 glioblastoma.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- High prevalence of focal and multi-focal somatic genetic variants in the human brain.Nature communications · 2018Article
- Article
- p53 mutations associated with aging-related rise in cancer incidence rates.Cell cycle (Georgetown, Tex.) · 2013Article
- Recent developments in oncolytic adenovirus-based immunotherapeutic agents for use against metastatic cancers.Cancer gene therapy · 2013Review
- Gene medicine for cancer treatment: commercially available medicine and accumulated clinical data in China.Drug design, development and therapy · 2009Article
- Apoptosis and proliferation: correlation with p53 in astrocytic tumours.Journal of neuro-oncology · 2005Article
- Genetic and hypoxic regulation of angiogenesis in gliomas.Journal of neuro-oncology · 2004Review
- Sensitizing glioma cells to cisplatin by abrogating the p53 response with antisense oligonucleotides.Cancer gene therapy · 2004Article
- Co-transduction of Apaf-1 and caspase-9 highly enhances p53-mediated apoptosis in gliomas.British journal of cancer · 2002Article
- Restoration of endogenous wild-type p53 activity in a glioblastoma cell line with intrinsic temperature-sensitive p53 induces growth arrest but not apoptosis.International journal of cancer · 2001Article
- Gene therapy for brain tumors.Current oncology reports · 2000Review
- Application of advances in molecular biology to the treatment of brain tumors.Current oncology reports · 2000Review
- p53 gene mutation and ink4a-arf deletion appear to be two mutually exclusive events in human glioblastoma.Oncogene · 2000Article
- Induction of medulloblastomas in p53-null mutant mice by somatic inactivation of Rb in the external granular layer cells of the cerebellum.Genes & development · 2000Article
- Hevin is down-regulated in many cancers and is a negative regulator of cell growth and proliferation.British journal of cancer · 2000Article
- Cells with TP53 mutations in low grade astrocytic tumors evolve clonally to malignancy and are an unfavorable prognostic factor.Oncogene · 1999Article
- No complementation between TP53 or RB-1 and v-src in astrocytomas of GFAP-v-src transgenic mice.Brain pathology (Zurich, Switzerland) · 1999Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 tumor suppressor gene (TP53) is the most frequently altered gene in human cancer and is also found mutated in several types of brain tumors. Loss of p53 function plays a central role in the development of cancer. The characterization of the biochemical pathways by which p53 alteration triggers tumorigenesis is the foundation for the design of novel therapeutic approaches. Investigations of the intracellular mechanisms at the origin of p53 tumor suppressive functions have shown that p53 is a transcription factor able to sense a variety of cellular insults and induce a dual response: cell growth arrest/senescence or apoptosis. Less well studied are p53's influences on extracellular events such as tumor angiogenesis, immunology and invasion. Here, we review these findings and specifically discuss their implications for brain tumor genesis, molecular diagnosis and prognosis. Of clinical importance are the findings that brain tumors with wild type (wt) or mutant p53 status may respond differently to radiation therapy and that novel therapeutic strategies using TP53 gene transfer or specifically targeting tumor cells with mutated p53 are being evaluated in clinical trials.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.